Administration Of Vitamin D Relieves Menstrual Pain

A new study published in the Archives of Internal Medicine suggests that vitamin D may relieve menstrual cramps. It was found that women with dysmenorrhea experiment no pain after receiving a single dose of vitamin D3, that is cholecalciferol.

Menstrual cramps, or dysmenorrhea, affects at least half of women of childbearing age and are caused  by prostaglandin, a hormone-like substance with a role in uterine contraction and relaxation of muscles and blood vessels. Dr. Jill Rabin, chief of obstetrics and gynecology at Long Island Jewish Medical Center in New Hyde Park vitamin, explains that vitamin D prevent the production of prostaglandins and furthermore, vitamin D has an anti-inflammatory effect. Dr. Rabin added that the study is only the first step and that it needs to be confirmed  by further research.

Woman with menstrual cramps

U.S. experts believe that it is too early to recommend high doses of vitamin D3 to women with menstrual pain, because the study did not show the potential long-term effects of vitamin D3. Dr. Robert Graham,  internist and vitamin D expert at Lenox Hill Hospital in New York City, noted that the study results are quite amazing but the required dose that needs to be administered is high.

The study used a relatively small sample: 40 women, who were divided into two groups, one receiving a single dose of 300,000 IU of vitamin D3, and one who received placebo for 5 days before the start of menstruation. After two months in the group receiving vitamin D3 there has been a 41% reduction in menstrual pain, while in the placebo group no changes war noticed. Also, none of the women who took vitamin D3 had no need to use NSAIDs, while in the placebo group, 40% of women had used NSAIDs. At the beginning of the study, patients had vitamin D blood levels 25% higher of normal. At the end of the study vitamin D blood levels were not reported.

The dose of 300,000 IU of vitamin D used in the study exceeds the usual dose of 600 IU daily recommended for women of childbearing age. The study also does not bring information about potential long-term effects of vitamin D, due to the study short period of only two months. Currently, dysmenorrhea is treated with NSAIDs, such as ibuprofen, and in persistent and severe pain cases with contraceptive pills. Both drugs have side effects such as stomach pain, bleeding disorders among others.

It is worth mentioning that other studies have also looked into the potential beneficial effects of vitamin D (the role of vitamin D in cancer, heart disease and autoimmune diseases).

Damaged Myelin Is Not The Cause Of Multiple Sclerosis

It is estimated that in the US alone, there are currently 400.000 people suffering from multiple sclerosis or MS. Worldwide there are more than 2.1 million diagnosed cases of multiple sclerosis. MS is a demyelinating disease (which leads to the disappearance of myelin, lipid substance that surrounds nerve fibers of the white matter) of the central nervous system, that leads to sclerosis (hardening caused by an abnormal deposition of connective tissue), appearing in the form of plates of white matter. Myelin is a soft substance that formes the nerve sheath and participates in the correct transmission of nerve electrical signals.

MRI image of a brain with multiple sclerosis

There are many assumptions without a scientific basis on the onset and development of multiple sclerosis and one of them, has now been proved to be incorrect by University of Zurich researchers: also known as the neurodegenerative hypothesis, the destruction of oligodendrocytes (cells that produce myelin) does not lead to multiple sclerosis.

The study which aimed to make the neurodegenerative hypothesis obsolete, was based on the fact that some patients presented some kind of myelin damage without the presence of an autoimmune disturbance. The neurodegenerative hypothesis claims that the immune system does not play a key role in triggering characteristic myelin damage and the autoimmune attack against myelin is the result and not the determining factor of the disease.

In order to prove this hypothesis wrong, scientists used mouse models in which, by altering the genetic code, they were able to damage the myelin without triggering an immune response. Myelin damage, very similar to that which can be observed in multiple sclerosis patients has not determined an MS-like autoimmune response in any mouse model. Next researchers tried to observe if an active immune defence due to a combination between infection and damage of the myelin leads to MS. The conclusion was firm: “We were unable to detect an MS-like disease “ no matter how intensely we stimulated the immune system,” says Ari Waisman, a professor from the University Medical Center Mainz. “We therefore consider the neurodegenerative hypothesis obsolete.”

Researchers expressed their wish to continue their work and eventually find the exact cause of multiple sclerosis focusing more on the immune system and less on the brain and spinal cord.

Noninvasive Method For Evaluating Down Syndrome Risk Discovered

Scientists at Aria Diagnostics in San Jose, have discovered a new method to detect chromosomal abnormalities . The recent statistical algorithm, DANSR/FORTE assay, can detect 21 and 18 trisomy using a noninvasive test performed on maternal blood. Unlike other genetic screening tests, this assay is more scalable and has the benefit of reducing the number of unnecessary amniocenteses.

Children born with trisomy 18 or trisomy 21 have different physical traits and a certain degree of mental handicap. Even if it can not be treated, children with Down syndrome can lead normal lives if the necessary care benefits are provided.

Aneuploidy or fetal chromosomal abnormalities can be diagnosed with invasive tests such as amniocentesis or chorionic villi sampling. Although accurate, these tests are expensive and, moreover, could induce miscarriage. Another technique, MPSS, massively parallel shotgun sequencing, examines cells without DNA from maternal plasma to detect trisomy 21, or Down syndrome, and trisomy 18, or Edwards syndrome. Even if it can accurately identify these abnormalities, one of the main shortcomings of MPSS is that it requires a lot of DNA sequencing.

Researchers at the Diagnostics area in San Jose, CA have developed a new test that searches only for certain chromosomes. That means it needs 10 times less DNA than MPSS.

With thys study, which will be published in the April issue of the American Journal of Obstetrics & Gynecology (AJOG), researchers have developed a new statistical algorithm, the fetal-fraction Optimized Risk of Trisomy Evaluation (FORTE â„¢), which correlates maternal age with the percentage of fetal DNA in the sample, thus obtaining a certain score for trisomy. Dr.Ken Song, MD, explains the idea of this algorithm. “The higher the fraction of fetal cfDNA, the greater the difference in the number of cfDNA fragments originating from trisomic versus disomic [normal] chromosomes and hence the easier it is to detect trisomy.’

To test the accuracy DANSR / STRONG assay, Dr. Song and his colleagues examined a sample of 123 normal pregnancies, 36 of T21 and 8 of T18. All cases were tested using DANSR / STRONG assay for detection of trisomy 18 and trisomy 21. The new testing method was accurate in all 36 cases of T21 and 8 cases of T18.

Kypros H. Nicolaides, MD, senior author of the University of London study draws attention to the fact that all cases tested so far were suspected to have a chromosomal abnormality. He added that it would be necessary to verify the accuracy of cfADN testing on the general population, where the risk of aneuploidy is much smaller.

New Compounds Effective Against Antibiotic Resistant Infections Discovered

A new class of compounds that can tackle antibiotic resistant infections with a reduced chance of developing resistance was discovered by reseachers at the University of Michigan. The results were published online in the Proceedings of the National Academy of Sciences.

After screening and testing several compounds, researchers from the Center Of Chemical Genomics discovered a new class of drugs that can inhibit the growth and spread of Group A Strep in mouse models. Their findings suggest that these small molecules could have similar effects in treating infections caused by group A Streptoccoccus in humans.

Some pathogens have acquired resistance to drugs due to too long or too short antibiotic treatment periods. Frequent administration of antibiotics has encouraged the emergence of resistant bacterial species and therefore of harder to treat infections. Antibiotic resistance is one of the major public health problems. The National Academy of Sciences estimated that such resistant infections cost U.S. society at least $4 to $5 billion each year.

Antibiotics in use today act by interfering with the bacterial metabolism to kill or stop its growth. Meanwhile better adapted strains can elude the antibiotic attack and continue to multiply.

When germs become resistant to certain antibiotics, the treatment scheme must be changed with other antibiotics combinations. This is only a temporary solution for. It is therefore very important that antibiotics to be prescribed and used rationally.

Penicillin

An alternate approach is to deprive bacteria from nitric oxide, making them vulnerable and therefore easier to kill. Thus, the required dose of antibiotics is lowered and less toxic to the body (following the exposure to antibacterial substances and antibiotics, bacteria produce nitric oxide, which makes them much stronger and more resistant to aggressive factors. One such aggressive factor are antibiotics, exercising an oxidative stress on the pathogens similar to the effect free radicals have on human tissues like tobacco smoke, pollution, food additives and so on.)

Combining conventional treatment options for Group A Streptococcal infections like penicillin with these newly discovered compounds can result in more effective ways to avoid the selection of antibiotic resistant strains and achieve better treatment results.

Malfunctioning Protein Linked To Obesity And Liver Disease

The researchers of the Imperial London College have conducted a study according to which the cause of liver disease and obesity is represented by malfunctions of a certain protein that is functioning as a dietary fat sensor. Their demonstrations emphasize the possibility of finding new drugs that can be used for treating metabolic disorders and obesity.

The culprit protein, GPR120, is located on the surface of the cells in the liver, gut and fat tissues and gives the cells the ability to detect and respond to the unsaturated fatty acids , mainly the omega-3 fatty acid which are known to have a very good impact on health. The researchers discovered through this study that mice short on GPR120 protein were more likely to develop obesity and liver diseases while being fed with high-fat food.  Another important finding of the study had to do with the fact that people having a certain mutation in the gene encoding this protein, thus stopping the GPR120 response to the omega-3 fatty acids, were more prone to become obese.

Faulty Protein

When the unsaturated fatty acid combined with the GPR120 protein in the gut, the hormones are released in order to decrease  the appetite and to stimulate the pancreas to generate the insulin. When the fatty cells feel the raised levels of fat in the blood, with the help of the GPR120 protein, they multiply in order to create more cells responsible for storing all the fat, thus decreasing the risk of fatty liver and furring of the arteries. This mechanism might represent an important way of highlighting some of the healthy  effects of the omega-3 acids.

When the lab mice were put on a diet based on high fat aliments, those individuals lacking the GPR120 not only  they have become obese but they also developed fatty livers, deficient control of blood glucose and lower numbers of fat cells. The scientists concluded that mice deficient in GPR120 have problems with the storage of the excess fat in the fat tissue. In return, their bodies deposit the fat in areas known to cause health disorders, such as the liver, the muscles and the walls of the arteries. For the human beings this form of obesity is associated with heart disease and type 2 diabetes.

The present study brought together scientists from Great Britain, France and Japan having the Professor Philippe Froguel, from the School of Public Health at Imperial College London, as the leader.

The gene of the GPR120 protein was analyzed on 6942 obese people and 7654 controls in order to discover if the differences in the code carrying the instructions for creating the protein, are responsible for the human obesity. Their resolution was that one mutation rendering the protein disorder increases a human’s obesity up to 60%. The researchers consider that the mutation of this protein echoes the effect of an unhealthy diet which lacks the unsaturated omega-3 fat.

Migrating Cells Can Make The Difference Between Left And Right

Researchers from UCLA discovered that cells prefer to turn right in their migration process when changes occur in their environment. They where also able to explain the processes that occurs inside cells when they are migrating and creating the left-right asymmetry in tissues. This left-right asymmetry is very important as this is the way in which differences between the right and left side structures like the brain or the hand are created.

The study provides a basis for discovering how to stimulate a patient stem cells to create a liver or a kidney or even a heart . Chances to manage to recreate tissue that is damaged by diseases like arthritis or osteoporosis are also high in the near future.

Researchers were able to create in the lab a culture surface for stem cells, using microtechnology. This culture surface contained stripes of protein substrates that present the capacity to be cell-adhesive or cell-repellent. This two types of stripes were placed alternatively on the culture surface. The scientists compared this culture surface with a floor that has alternating narrow horizontal stripes of carpet and tile. This type of surface can be observed in human tissues when cells are migrating.

In their migration process, when cells reach the interface between cell-adhesive and cell-repellent stripes, they present a tendency to turn right with a angle of 20 degrees and after this right turning, the cells lined up in long parallel rows. After this alignment, the cells produced diagonal stripes over the entire surface.

Cell Culture

These findings are very impressive because there was no clue that the cellular surface will trigger a right-left asymmetry in the migration of cells. In addition, vascular cells that were used for this study spontaneously formed structures in the culture. The conclusion was that cells can sense substrates on which they are growing  and the surface on which they proliferate can influence both cell migration and future structures that will be formed. An other interesting fact was the response of the cells to the horizontal stripes when they reorganized into diagonal stripes.

Scientists now hope to able to exploit these new findings and use cellular substrates that can interfere with the cell migration and proliferation process by instructing them to produce tissue or structures that are needed for replacement.

The next logical step would be trying to guide cells to organize into the desired two-dimensional structures and even into three-dimensional structures. Future applications of this study may help scientist engineer organs from patient’s stem cells, an important step forward in the organ transplantation field, considering nowadays the shortage of donor organs and the possible complications like graft-versus-host disease.

Scar Tissue Caused By Heart Attack Can Be Reversed Using Stem Cells

Soon the heart damage resulted after a heart attack can be considerably reversed using stem cells extracted from the patient’s own heart. During a heart attack, the heart muscle is deprived of oxygen due to the formation of a blood clot. Therefore, even if the patient’s heart heals after this unfortunate event, a scar tissue is formed and that the heart pumping function is affected. For this reason, researchers worldwide are working to find a way to heal heart tissue and improve heart function resulted from prolonged ischemia.

Scientists at Cedars-Sinai Heart Institute performed a study to determine whether stem cells extracted from the patient’s own heart can help repair the newly formed scar tissue . The study was conducted on a group of 25 patients. One month after suffering a heart attack, patients underwent a special procedure during which a tube into a vein in the neck to reach the heart was inserted and a sample of heart tissue was removed. Stem cells from the tissue sample were then grown in the laboratory. When researchers managed to obtain about 25 million cells, they  injected the stem cells back in the arteries surrounding the heart of the patient.

Cardiac Stem Cell

The research found that after the heart attack about 24% of the left ventricular was represented by scar tissue. This percentage went down after 6 months of treatment to 16%. Subsequently, a year after the procedure, the results showed that scar tissue accounted for only  12% of the left ventricle.

Scientists stated that stem cells “have an unprecedented ability to reduce scar and simultaneously stimulate the regrowth of healthy [heart] tissue”. Although the research main objective was to test the safety of the method, scientists also observed during this particular study how stem cell therapy stimulates healthy tissue growth and promotes scar tissue removal .

Over a decade of cell therapy trials failed to achieve comparable results until now. According to study author Dr. Eduardo Marban, he and his team are the first to record such a success. Effects are substantial and the results are better than they were in the animal testing phase.

However, even if stem cells manged to restore ventricular total capacity, the ejection fraction remained unchanged (amount of blood ejected with each beat from the left ventricle). Furthermore, other scientists who recognize the findings as very promising, suggest that the study was conducted on a very small sample of patients and therefore further research on larger samples is required for more accurate data.

Unconscious Learning Of High-Performance

According to a new study, a person’s brain patterns could be modified and his performances improved just by watching a computer screen. A new learning  method was discovered by scientists that uses decoded MRI imaging to modify brain performance. This method could also be used to help patients recuperate from different types of injuries or accidents or even learn a foreign language of fly an airplane. The study was published on December 8 in the journal Science.

The study, conducted at Boston University and  ATR Computational Neuroscience Laboratories in Kyoto, Japan has proven that using a patient’s visual cortex, scientists can induce brain activity patterns to match a state that was previously known and thereby enhance visual performance

Just imagine a person looking at a computer screen and modifying his brain patterns to match a sportsman or recuperate from spinal injury. Although scientists are not there yet, they suggest that such possibilities may soon be reality.

“Adult early visual areas are sufficiently plastic to cause visual perceptual learing,” according to Takeo Watanabe, neuroscientist and lead author

Scientists have discovered that pictures are gradually filled in a person’s brain,  appearing at the beginning as lines then edges, shapes, different colors and motion in early visual areas. The images are then filled in with more details making a blue pyramid appear as a blue pyramid for example. Scientists analyzed the early formation of different early visual areas, to observe their ability to improve learning and visual performance.

Previous research established a link between changes in early visual areas and improved visual performance while other studies evidentiated a link between higher visual areas and decision areas. No study has proven so far that early visual areas are sufficiently plastic to cause visual perceptual learning.

Post-doctoral fellow Kazuhisa Shibata created a method using decoded Functional magnetic resonance imaging neurofeedback to determine a certain activation pattern in targeted early visual areas that were linked to a pattern evoked by a specific visual feature in a desired region of the brain. Scientists then tested to see if repeation the activation pattern led to visual performance improvement. The result was a new learning method, effective enough to cause long-term improvements in tasks that are based on visual performance. The really surprising thing is that the test person was not aware of what he was actually learning.

Currently the decoded neurofeedback learning method might be used for different types of learning such as memory, motor and rehabilitation.

Cocaine-Induced Adaptive Behaviour Can Be Reversed Using Optogenetics

A team of Swiss scientists at the University of Geneva, has proven for the time that cocaine use is linked to physical brain changes. The study was led by Christian Lüscher and was published yesterday in Nature Magazine. The researchers also discovered methods that can be used to reverse the impact which cocaine has on the brain.

It is not a new thing that the firing potential of neurons that can be found in the nucleus accumbens (plays a central role in the reward circuit) is dramatically increased. The effects of cocaine like paranoia, delusions of persecution, visual hallucinations, auditory and tactile, increasing irrational acts, anger, distrust, depression and lack of motivation were long suspected to be caused by this increased neuronal firing potential but until now it has never been fully proven.

In order to prove the link between cocaine use and physical brain changes and also find a way to fight the effect of cocaine, Lüscher turned their attention to optogenetics process in which certain kinds of algae (which poses light-sensitive ion channels) are used to trigger a celular response to light. This property was used in this case to reduce the firing potential of neurons that was being increased by to cocaine use.

In their experiment, researchers expressed such light-sensitive ion channels in cortical neurons that normally communicate with neurons in the accumbens in laboratory mice that were administered several doses of cocaine. Then, the researchers fired laser pulses, causing a virtual storm of electrical impulses between the two types of neurons resulting in overkill, fact that determined the neurons to reduce their firing in response. This result effectively nullified the initial effect caused by the cocaine.

Optogenetics

By repeating their experiment  using several mice, and finding the same encouraging results each time (reduced firing potential of neurons and improved cocaine addiction specific behavior), researchers were able to establish a link between the two

While it seems that researches have found an effective method that can help cocaine addicts, it is not as simple as that. This particular techniques appears to be effective in mice that are newly addicted and whose brains have not changed dramatically.

Scientists Discovered New Multiple Sclerosis Protective Mechanism 

A team of researchers led by Alexander Prat and Jorge Alvarez at the University Of Montreal Hospital Research Center were able to decode how the blood-brain barrier is able to prevent the penetration of immune system cells into the brain. The study was published in the Science journal and researchers empathize that this findings regarding the blood-brain-barrier can help them to understand which are the mechanisms used by the brain to achieve a natural defence against the aggression of the immune system (which occur in the case of multiple sclerosis).

Multiple sclerosis is a debilitating auto-immune disease of the central nervous system, with inability of the brain-blood barrier to restrict and to control the passage of immune system cells into the brain. The result of this penetration of immune cells into the brain is that neurons in the brain and in the spinal cord cannot realize effective connections between them, leading therefore to extensive and recurrent damage of the central nervous system. Damage of the central nervous system leads to the occurrence of specific symptoms of multiple sclerosis, which include numbness, paralysis, visual problems, difficulties in coordination, moving and in balance. In the end, multiple sclerosis will lead to a chronic clinical handicap. There is no known treatment for this debilitating disease which affects the central nervous system.

Multiple Sclerosis New Protective Mechanism

The brain-blood barrier is a metabolic and physical barrier that has an important role in preventing the passage of harmful and unwanted cells or molecules into the central nervous system. This barrier is formed by endothelial cells (cells that are lining the interior surface of the blood vessels), which bound tightly and astrocytes (cells of the nervous system that have an important role in the transmission of the electrical signals in the brain and spinal cord).

The researchers were able to demonstrate that astrocytes are secreting a protein that has an important role in the organization of the central nervous system, called Sonic hedgehog and the endothelial cells present on their surfaces Hedgehog receptors. This two cells have an important role in the proper formation of the brain-blood barrier, during embryonic development and in maintaining the integrity of this barrier during adulthood.

More important, the scientists were able to demonstrate, using animal and human brain cells, that Hedgehog pathway has an important role in decreasing the migration of immune system cells into the central nervous system and in decreasing the adhesion of this type of cells. This means that the Hedgehog pathway is helping the brain-blood barrier to prevent the penetration of immune cells into the brain realizing therefore an anti-inflammatory balance of the central nervous system, when subjected to a direct attack of the immune system.

With this findings, the researchers hope that in the near future they will realize a proper therapeutic approach that will able to control the migration of immune system cells into the brain, finding this way, an efficient treatment for patients suffering from multiple sclerosis.